Oncornaviruses produced by murine leukemia cells in culture

Nowinski, Robert C.; Hays, Esther F.; Doyle, Theresa; Linkhart, Susan G.; Medeiros, Edward; Pickering, Ruth

doi:10.1016/0042-6822(77)90152-0

Cited by 54 publications

(29 citation statements)

References 7 publications

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“…The env gene products of MuLV (32) are expressed in a variety of tumor cells, including B16 melanoma (26), lymphomas and leukemias of high MuLV titer strains of mice (33)(34)(35), and simian virus 40-transformed NIH 3T3 cells (36). We have found that (i) CT26 expresses the MuLV env gene product while it is silent in the normal tissues of BALB/c mice, and (ii) this viral antigen, gp7O, serves as a potential tumor rejection antigen for the immune system.…”

Section: Discussionmentioning

confidence: 99%

The immunodominant major histocompatibility complex class I-restricted antigen of a murine colon tumor derives from an endogenous retroviral gene product.

Huang

Gulden

Woods

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

357

348

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Section: Discussionmentioning

confidence: 99%

The immunodominant major histocompatibility complex class I-restricted antigen of a murine colon tumor derives from an endogenous retroviral gene product.

Huang

Gulden

Woods

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

357

348

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“…Prehn, 1975;Hewitt et al, 1976 It is now accepted that all mice, laboratory and feral, contain murine leukaemia viral peptides built into the genome, and serum antibodies thereto (Nowinski, 1975 (Klein, 1975). However, there is now evidence that the inherited virus or proviruses may per se be relatively harmless and that a variant may be responsible for oncogenicity (Nowinski et al, 1977 Klein et al (1962).…”

Section: Discussionmentioning

confidence: 99%

Radiation leukaemogenesis: is virus really necessary?

Loutit¹,

Ash²

1978

Br J Cancer

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Generalized lymphosarcomatosis (leukaemia) of non-thymic type occurs in mice bearing 90Sr or 239Pu or 226Ra. Tumours passaged from such mice have been tested for tumour-associated transplantation antigens that could provoke a protective immunity which would be expected if such antigens were determined by virus activated by the irradiation. Sub-threshold doses of living syngeneic tumour, large doses of living allogeneic tumour and large doses of killed syngeneic tumour were without protective effect. This suggests that viruses observed electron micrographically in such tumours are passengers and not causative. Images Fig. 1 Fig. 2 Fig. 3

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“…Such supernatants were also employed to determine the presence of reverse transcriptase enzymatic activity according to published methods [13,191. Virus was collected and concentrated from such supernatants by centrifugation at 40000 rpm for 35 min using an SW50.1 rotor.…”

Section: Viral Assaysmentioning

confidence: 99%

The specificity of H‐2‐restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus‐induced tumors II. Altered gp70 display and production of noninfectious virus particles by an insusceptible variant tumor

Green

Brown

1983

Eur J Immunol

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Derived from the susceptible AKR.H-2bSL1 tumor cell line, a variant tumor subclone, cl.18-5, was selectively insusceptible to H-2-restricted anti-AKR/Gross virus cytotoxic T lymphocytes (CTL) due to its failure to be recognized. In this study, the expression of virus-related products by variant cl.18-5 cells was compared to that of AKR.H-2bSL1 cells and a susceptible clone, as an approach towards defining the virus-associated antigens recognized by anti-AKR/Gross virus CTL. Despite the type specificity of the CTL, cl.18-5 displayed normal levels of the group-specific antigen (gag) encoded proteins p30, p15, p12 and p10, and the gag-associated Gross cell surface antigen. These results were confirmed by fluorescence-activated cell sorter analysis employing monoclonal antibodies specific for either AKR p12 or the cell surface glycosylated form of AKR ecotropic gag product. In contrast, cl.18-5 was variably less sensitive than AKR.H-2bSL1 to the action of complement and xenogeneic antisera directed against the envelope (env) product gp70. In addition, a panel of five monoclonal antibodies to gp70, which detect distinct endogenous ecotropic viral determinants, lysed AKR.H-2bSL1, but not cl.18-5 cells. However, absorption experiments indicated that cl.18-5 did express near normal levels of these specificities, suggesting an alteration in the orientation or topographical distribution of these determinants. Consistent with an inappropriate display of env products, cl.18-5 was found to be deficient in the production of infectious ecotropic leukemia virus. The particulate fraction of the cell-free supernatant of cl.18-5 contained normal levels of reverse transcriptase activity, indicating that noninfectious viral particles were being produced. Collectively, these results point to an association between recognition by anti-AKR/Gross virus CTL and the expression of ecotropic gp70 required for infectivity of virus.

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Oncornaviruses produced by murine leukemia cells in culture

Cited by 54 publications

References 7 publications

The immunodominant major histocompatibility complex class I-restricted antigen of a murine colon tumor derives from an endogenous retroviral gene product.

The immunodominant major histocompatibility complex class I-restricted antigen of a murine colon tumor derives from an endogenous retroviral gene product.

Radiation leukaemogenesis: is virus really necessary?

The specificity of H‐2‐restricted cytotoxic T lymphocytes directed to AKR/Gross leukemia virus‐induced tumors II. Altered gp70 display and production of noninfectious virus particles by an insusceptible variant tumor

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